SpectraCell Blog

The prevalence of AD in our aging population is frightening, affecting 10% of those over age 60, 20% of those over age 70, and 30% of those over age 80.1There are roughly 5 to 6 million AD patients in the US and an equal number of people with mild cognitive impairment (MCI), memory loss, but not enough loss of function to be called AD. In general, MCI is a precursor to AD, with 80% eventually developing AD, at the rate of 15% per year.2

Supplementation with Zinc

Because this was an animal study, researchers could precisely manipulate and consequently correlate blood and brain levels of zinc and copper and with age and cognitive function. Specifically, they measured the effect of zinc supplementation on short-term memory, long-term memory and spatial memory. In addition, they measured zinc and copper levels in both the blood and the hippocampus, which is the part of the brain linked to memory.

The authors discovered that as the rats got older, their blood levels of copper increased while blood levels of zinc decreased with simultaneous decreases in memory. However, supplementation with zinc reversed the elevated copper levels and improved memory in all areas. It is well established that zinc and copper work together and that balance of the minerals is important. In fact, excess zinc supplementation may possibly induce a copper deficiency, so although this study concludes “zinc as a plausible therapeutic intervention” for age-related cognitive decline, this study reminds us that micronutrients do not work alone but in balance so a comprehensive look at nutritional status is key.

In this provocative mouse study, researchers demonstrated that marginal vitamin A deficiency in utero may have large implications on cognitive function later in life, particularly in the development of Alzheimer's disease. It revealed that vitamin A deficiency increases the potential for amyloid beta to form in the brain, a hallmark of Alzheimer’s disease. Amyloid beta is a type of protein that forms tangles in the brain of Alzheimer’s patients, eventually leading to plaque formation and ultimately manifesting as major cognitive dysfunction and severe memory loss.

Specifically, amyloid precursor protein (generally benign when it stays intact) becomes amyloid beta when it is acted upon by a special enzyme that cleaves it. Vitamin A deficiency increases the activity of this enzyme, thus increasing the production of amyloid beta in the brain. When therapeutic doses of vitamin A was administered to mice, memory was restored, suggesting that “vitamin A supplementation might be a potential approach for Alzheimer’s disease prevention and treatment.”